Mutation as a Stress Response and the Regulation of Evolvability
- 1 January 2007
- journal article
- review article
- Published by Taylor & Francis Ltd in Critical Reviews in Biochemistry and Molecular Biology
- Vol. 42 (5), 399-435
- https://doi.org/10.1080/10409230701648502
Abstract
Our concept of a stable genome is evolving to one in which genomes are plastic and responsive to environmental changes. Growing evidence shows that a variety of environmental stresses induce genomic instability in bacteria, yeast, and human cancer cells, generating occasional fitter mutants and potentially accelerating adaptive evolution. The emerging molecular mechanisms of stress-induced mutagenesis vary but share telling common components that underscore two common themes. The first is the regulation of mutagenesis in time by cellular stress responses, which promote random mutations specifically when cells are poorly adapted to their environments, i.e., when they are stressed. A second theme is the possible restriction of random mutagenesis in genomic space, achieved via coupling of mutation-generating machinery to local events such as DNA-break repair or transcription. Such localization may minimize accumulation of deleterious mutations in the genomes of rare fitter mutants, and promote local concerted evolution. Although mutagenesis induced by stresses other than direct damage to DNA was previously controversial, evidence for the existence of various stress-induced mutagenesis programs is now overwhelming and widespread. Such mechanisms probably fuel evolution of microbial pathogenesis and antibiotic-resistance, and tumor progression and chemotherapy resistance, all of which occur under stress, driven by mutations. The emerging commonalities in stress-induced-mutation mechanisms provide hope for new therapeutic interventions for all of these processes.Keywords
This publication has 130 references indexed in Scilit:
- Spontaneous DNA breakage in single living Escherichia coli cellsNature Genetics, 2007
- Evidence for mutation showersProceedings of the National Academy of Sciences of the United States of America, 2007
- Regulation of Bacterial RecA Protein FunctionCritical Reviews in Biochemistry and Molecular Biology, 2007
- Human cancers express a mutator phenotypeProceedings of the National Academy of Sciences of the United States of America, 2006
- Multiple pathways of selected gene amplification during adaptive mutationProceedings of the National Academy of Sciences of the United States of America, 2006
- The PhoP/PhoQ two-component system stabilizes the alternative sigma factor RpoS in Salmonella entericaProceedings of the National Academy of Sciences of the United States of America, 2006
- Non-homologous end-joining factors of Saccharomyces cerevisiaeFEMS Microbiology Reviews, 2004
- Adaptive Amplification: An Inducible Chromosomal Instability MechanismCell, 2000
- Asymmetries Generated by Transcription-Coupled Repair in Enterobacterial GenesScience, 1996
- Evidence that F Plasmid Transfer Replication Underlies Apparent Adaptive MutationScience, 1995